Lymphocytes bearing the γδ T cell receptor in acute Brucella melitensis infection
✍ Scribed by Alberto Bertotto; Roberto Gerli; Fabrizio Spinozzi; Christopher Muscat; Francesco Scalise; Giuseppe Castellueei; Maddalena Sposito; Francesco Candio; Renato Vaeearo
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Volume
- 23
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
Abstract
A phenotypical analysis carried out by indirect immunofluorescence and two‐color cytofluorometry showed that the number of lymphocytes bearing the γδ T cell receptor (TcR) heterodimer was dramatically increased in the blood of six children with Brucella melitensis infection. Most in vivo expanded γδ T cells reacted with a monoclonal antibody which identifies Vδ2 gene products and a significant proportion expressed CD25 and HLA‐DR activation antigens. In addition, whereas only a few γδ T lymphocytes were CD8^+^, nearly all were CD4^−^. Highly enriched populations of both αβ and γδ T cells were obtained by negative immunoselection from three subjects with brucellosis sampled during convalescence. Despite the different form of their TcR, the proliferation of these two major T cell subsets in response to a mitogenic anti‐CD3 monoclonal reagent (OKT3) was optimal. In contrast, αβ, but not γδ, T lymphocytes proliferated vigorously in response to the antigenic stimulus elicited by heat‐killed Brucella. Further studies are, therefore, needed to determine whether the selective expansion of the γδ T cell subpopulation observed during the clinical course of the infection is driven by antigenic determinant(s) borne by the pathogen in vivo or is due to host‐derived stimuli, such as autologous heat‐shock proteins expressed on the surface of the infected cells.
📜 SIMILAR VOLUMES
## Abstract In order to clarify the cellular tropism of human T‐cell leukemia virus type I (HTLV‐I) and the effects of HTLV‐I infection on T‐cell functions, we investigated the infectiousness of HTLV‐I on T cells bearing T‐cell receptor (TCR) γδ and functional alterations of the HTLV‐I‐infected TCR